Cardiovascular disease is the most lethal complication for the more than 10 million patients in the United States who suffer from diabetes mellitus. In experimental models of type 1 diabetes, hypoinsulinemia has profound effects on myocardial perfusion, fatty acid metabolism, and function. It is unknown if these observations are applicable to the human condition our hypothesis is that in patients with type 1 diabetes 1) hypoinsulinemia impairs myocardial perfusion, and increases the reliance on fatty acid utilization to support overall oxidative metabolism which impairs systolic function particularly when myocardial work in increased; and 2) interventions that decrease the reliance on fatty acid utilization will have salutary effects on myocardial mechanical function, particularly when myocardial work in increased. We will prove or disprove this hypothesis by addressing the following specific aims: 1. To verify whether myocardial glucose utilization can be determined more accurately from the myocardial kinetics of 1-/11C-glucose or 18F- fluorodeoxyglucose measured by PET in a well-controlled canine model: 2. To determine in humans with type 1 diabetes in myocardial perfusion reserve is impaired which leads to an impairment in myocardial mechanical function at rest and during pharmacological stress and to assess the relative contributions of hyperglycemia and hypoinsulinemia to this phenomena. 3. To determine in humans with type 1 diabetes the importance of plasma fatty acid levels on the proportional contribution of myocardial fatty acid to overall oxidative metabolism and its impact on mechanical function at rest and during pharmacological stress. 4. To determine in humans with type 1 diabetes the importance of plasma insulin levels on the proportional contribution of myocardial fatty acid to overall oxidative metabolism and its impact on mechanical function at rest and during pharmacological stress.